HEPATIC INSULIN AND GLUCAGON RECEPTORS IN PREGNANCY - THEIR ROLE IN THE ENHANCED CATABOLISM DURING FASTING

The response to dietary deprivation in late pregnancy, as compared to the nonpregnant condition, is more rapid and profound in terms of mobilization of fuels from peripheral tissues, hepatic ketogenesis and gluconeogenesis (accelerated starvation). The potential role of hepatic insulin and glucagon receptors in mediating these changes by comparing 48-h fasted 18-day pregnant and age-matched non-gravid rats was examined. Molar ratios for insulin:glucagon in peripheral and portal blood were significantly higher in the pregnant rats. Insulin binding to purified liver plasma membrane receptors, when appropriately corrected for differences in insulin degradation by the membrane system, was marginally diminished in the pregnant animals. Glucagon binding and adenylate cyclase activation by glucagon was indistinguishable in the 2 groups of animals. Based on portal vein hormone concentrations and the values for receptor binding, liver insulinization relative to glucagonization appears to be unchanged or slightly increased in the fasted pregnant rat compared to the fasted nongravid rat. It seems unlikely that much of the accelerated starvation response in late pregnancy can be ascribed to diminished insulin and/or increased glucagon availability at the hepatocellular level. Instead, postreceptor events apparently play the major role in sustaining the intrahepatic realignments of established fasting in late pregnancy.